This animal research is designed to model a clinical problem: Sudden death occurs in the majority of children who die late postoperatively after repair of congenital heart defects such as tetralogy of Fallot (TOF). In our studies on such patients, those who died suddenly had the combination of ventricular dysrythmias and persistently elevated RV systolic and end-diastolic pressures. In this research, we will use chronically instrumented beagles and create a model of "preoperative" cyanotic TOF and then later perform "correction" with varying hemodynamic residuae. The specific aims are to determine: 1) The anatomic and physiologic conditions necessary for the development of ventricular dysrhythmias; 2) The cellular electrophysiologic mechanisms of the dysrhythmias. Our previous animal research has suggested that these dysrhythmias might involve triggered activity; 3) The mechanisms for sudden death. Three groups of animals will be used: 1) control animals (four subgroups each with 6 animals) at the age of 6 weeks will undergo either a) PA banding (PAB), b) pulmonary artery to left atrium anastomosis (ANAS), c) combination, or d) sham op, and at 6 months, instrumentation with 9 pairs of epicardial electrodes. 2) The "PO-TOF- hemodynamics" will have both PAB and ANAS at 6 weeks, and at 6 months will undergo instrumentation and right ventriculotomy, plus combinations of debanding, closure of ANAS and pulmonary valvectomy. 3) The "PO-TOF-ventriculotomy" (2 subgroups) will have "repair" without ventriculotomy. After the second op, every two weeks for six months, electrophysiology study will be performed without sedation, and 24 hour ECGs will be done. At 12 months, the hemodynamic response of the unsedated animal to supraventricular tachycardia (rapid atrial pacing), VT (rapid ventricular pacing) and exercise (isoproterenol) will be examined with previously implanted catheters, as well as the blood flow to the myocardium, brain and kidneys with radioactive microspheres. The heart will be excised and microelectrode studies will be performed on the RV free wall with the same extrastimulus protocol as in the intact animal. The significance is: 1) If certain residual hemodynamic abnormalities are found to be associated with dysrhythmias (e.g. pulmonary insufficiency) they could be avoided. 2) If a specific mechanism for dysrhythmias due to hypertrophy and fibrosis is found, this might extend to lesions such as aortic stenosis or systemic hypertension. This difference in mechanism could account for the difference in drug response between certain children and adults with VT. 3) If the mechanism for the dysrhythmias involves triggered activity, this would be the first chronic animal model of this dysrhythmia. 4) If the explanation for sudden death from VT can be found, this will benefit both children and adults since it might be possible to predict which patients will die suddenly.